Endocytic pathways of SR-A CAVEOLAE-DEPENDENT ENDOCYTOSIS IS REQUIRED FOR CLASS A MACROPHAGE SCAVENGER RECEPTOR-MEDIATED APOPTOSIS IN MACROPHAGES

نویسندگان

  • Xu-Dong Zhu
  • Yan Zhuang
  • Jing-Jing Ben
  • Ling-Ling Qian
  • Han-Peng Huang
  • Hui Bai
  • Jia-Hao Sha
  • Zhi-Gang He
  • Qi Chen
چکیده

CAVEOLAE-DEPENDENT ENDOCYTOSIS IS REQUIRED FOR CLASS A MACROPHAGE SCAVENGER RECEPTOR-MEDIATED APOPTOSIS IN MACROPHAGES Xu-Dong Zhu, Yan Zhuang, Jing-Jing Ben, Ling-Ling Qian 2 , Han-Peng Huang , Hui Bai, Jia-Hao Sha, Zhi-Gang He 1,2 and Qi Chen From the Institute of Reproductive Medicine and Atherosclerosis Research Centre, Key Laboratory of Human Functional Genomics, Nanjing Medical University, Nanjing, People’s Republic of China, and Division of Neuroscience, Children’s Hospital, Harvard Medical School, Boston, Massachusetts Running head: Endocytic pathways of SR-A Address correspondence to: Qi Chen, Atherosclerosis Research Centre, Key Laboratory of Human Functional Genomics, Nanjing Medical University, Nanjing 210029, People’s Republic of China. Telephone: +86 25 86862610, Fax: +86 25 86508960; E-mail: [email protected]

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Caveolae-dependent endocytosis is required for class A macrophage scavenger receptor-mediated apoptosis in macrophages.

SR-A (class A macrophage scavenger receptor) is a transmembrane receptor that can bind many different ligands, including modified lipoproteins that are relevant to the development of vascular diseases. However, the precise endocytic pathways of SR-A/mediated ligands internalization are not fully characterized. In this study, we show that the SR-A/ligand complex can be endocytosed by both clathr...

متن کامل

Endocytic uptake of advanced glycation end products by mouse liver sinusoidal endothelial cells is mediated by a scavenger receptor distinct from the macrophage scavenger receptor class A.

Previous studies with peritoneal macrophages obtained from macrophage scavenger receptor class A (MSR-A) knock-out mice showed that the endocytic uptake of advanced glycation end products (AGE) by macrophages was mediated mainly by MSR-A. However, it is controversial whether the endocytic uptake of intravenously injected AGE proteins by liver sinusoidal endothelial cells (LECs) is similarly exp...

متن کامل

Signaling pathways initiated in macrophages after engagement of type A scavenger receptors.

Scavenger receptors are macrophage cell surface molecules associated with endocytic uptake of lipoproteins and binding of microbial ligands. Macrophage class A scavenger receptors (SR-As) interact with ligands to induce cellular signaling leading to gene transcription and cytokine release. We used inhibitors of early and late signaling to block SR-A-mediated polyinosinic-polycytidilic acid (pol...

متن کامل

Class A scavenger receptor activation inhibits endoplasmic reticulum stress-induced autophagy in macrophage

Macrophage death in advanced atherosclerosis promotes plaque necrosis and destabilization. Involvement of autophagy in bulk degradation of cellular components has been recognized recently as an important mechanism for cell survival under endoplasmic reticulum (ER) stress. We previously found that the engagement of class A scavenger receptor (SR-A) triggered JNK-dependent apoptosis in ER-stresse...

متن کامل

M-CSF-induced macropinocytosis increases solute endocytosis but not receptor-mediated endocytosis in mouse macrophages.

Although coated vesicles can mediate both solute and receptor-mediated endocytosis, there are other kinds of endocytic vesicles that contribute to these processes. The relative contributions of these other organelles, particularly regarding solute influx, remains unsettled. Here we describe a physiological uncoupling of solute and receptor-mediated endocytosis that occurs during growth factor-s...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2010